Perioperative fracture treatment complicated by fracture blisters remains a topic of

controversy. These blisters may delay surgery, alter the optimum treatment plan, promote
wound infection, delay wound healing, and ultimately prolong recovery. Fracture blisters
may appear as early as six hours after injury or as late as three weeks after trauma. These
blisters signify underlying soft tissue damage and may result in increased infection rates
for both operatively and nonoperatively treated fractures. Treatment recommendations
have consisted of benign neglect, debridement, aspiration and surgical delay until
reepithelialization occurs.
What are Fracture Blisters?
Fracture blisters are defined as skin bullae and blisters representing areas of epidermal
necrosis with separation of the stratified squamous cell layer by edema fluid.
Two types of fracture blisters have been identified: clear fluid-filled and blood-filled. The
blood-filled blisters have been shown histologically to have complete separation of the
dermis from the epidermis, whereas the clear fluid-filled blisters demonstrate partial
epidermal separation of the epidermis from the underlying dermis, with a few scattered
areas of retained epithelial cells on the dermis.
It is believed that blood-filled blisters are the result of injury to the papillary vasculature,
allowing blood to escape into the blister these represent a more significant injury
histologically and clinically. Due to detachment of the epidermis from the underlying
dermis, eventual necrosis of the epidermis often ensues. Edema and venous stasis
resulting from the injury induce collapse and thrombosis of affected blood and lymphatic
vessels, thus adding to circulatory compromise.
Fractures blisters contain sterile fluid but demonstrate colonization with multiple
organisms once ruptured. Staphylococcus epidermidis and aureus were the most
commonly cultured organisms. Infection has been shown to occur when blister beds were
inoculated with as few as 100 organisms or less. Bacterial colonization was shown to be
present until reepithelialization. This coupled with the resultant epidermal necrosis and
hypoxia, leads to an increased susceptibility to wound infection and dehiscence that is
double the overall complication rate compared to fractures void of blistering.
Fracture blisters are found in areas with bony prominences and where there is an absence
of well formed adipose or muscular layers. The elbow, foot and distal tibia have the
greatest incidence of fracture blistering. In a study by Varela et al, the foot and ankle
comprised 44.5% of all fracture blisters. The ankle is particularly vulnerable to trauma
and skin breakdown due to flatter epidermal papillae, sparse subcutaneous tissue and an
extensive venous network. Open fractures and early ORIF rarely demonstrate fracture
blisters due to wound decompression.
Treatment and Prevention
The foot and ankle surgeon must identify those individuals at risk for developing fracture
blisters and direct treatment toward prevention. Immobilization, edema control with
compression and elevation, and cryotherapy are essential in the prevention of skin
breakdown. These simple steps help reestablish the normal pathways for blood and
lymphatic circulation. Early ORIF also helps prevent fracture blistering by placing the
tissues and vessels back in proper alignment and by providing early decompression.
Fracture blister prevention is not always possible. When fracture blisters are discovered,

there are a variety of treatment options: application of a dry compressive dressing and
splinting, aspiration, deroofing, and benign neglect have all been described. In a study by
Giordano et al, no significant differences were found in blister healing with the various
treatment techniques. However, triple antibiotic ointments (Neosporin, Bacitracin,
Polysporin) have been shown to enhance wound healing as opposed to harsher agents
such as iodine or hydrogen peroxide, which interfere with epidermal reepithelialization.
The time to reepithelialization occurs from 4-20 days after blister formation and is
considered complete when a moist dermal layer or granulation-type tissue is covered by
an epithelial layer, and the blister bed is no longer sensitive to touch.
Hemorrhagic fracture blisters
Timing of surgical intervention after blister discovery remains controversial. In Varela's
study, patients who underwent open reduction internal fixation within 24 hours of injury
had the lowest incidence of fracture blisters, but this is not always feasible. Often,
fracture blisters are first discovered 2-3 days after injury and prior to surgical
intervention. Giordano et al reported on 53 fractures complicated by overlying fracture
blisters and showed no complications when incisions were made through clear, fluidfilled blisters or when made adjacent to either blister type. However, other authors have
advocated avoiding incisions through either blister, as the blister may indicate injury to
the deeper soft tissues, and extend beyond the actual edges of the blister. Most surgeons
do agree on the avoidance of blood-filled blisters as any incision directly through these
provides postoperative colonization of the blister bed and direct colonization of the
surgical wound. Giordano shows a statistically significant difference in the wound
healing complication rate between blood and clear fluid-filled blisters, with all
complications occurring in the blood-filled group.
At our institution, once fracture blisters are discovered, they are decompressed but not
deroofed under sterile conditions, followed by the application of bacitracin, vaseline
gauze and a compressive dressing. Surgery is often delayed 7-10 days to allow for
reepithelialization. External fixation may be employed in high energy trauma and with
impending edema with or without the presence of fracture blisters, to allow for reduced
tension on the soft tissues and edema control, until definitive internal fixation can be
performed. Surgery will be delayed up to 3 weeks, at which time a decision is made to
treat by closed means or proceed with ORIF and accept some degree of wound
complications in order to avoid malunion or malreduction of the fracture.
Fracture blisters are tense bullae that arise in areas with little soft tissue between the bone
and skin. Although the blister fluid is sterile, once ruptured, rapid bacterial colonization
may ensue. Clear fluid-filled blisters show scattered areas of retained epithelial cells that
may aid in faster reepithelialization ( Regrowth of epithelial tissue over a denuded
surface. Surgical placement of a graft of epithelium over a denuded surface ) as compared
to blood-filled blisters. It appears that there is no statistical difference in blister healing
with the various treatment techniques. Delayed operative fixation can probably be
performed safely through either clear fluid-filled or blood-filled blisters. Early operative
fixation, however, should not place incisions through blood-filled blisters and caution
should be used with clear fluid-filled blisters as the injured soft tissue may extend beyond
the blister edges.
In high energy injuries, the foot and ankle surgeon must anticipate concomitant soft tissue

injury such as fracture blisters. When early ORIF is not feasible and prevention is
unsuccessful, the surgeon must be knowledgeable of the pathophysiology of blistering
and the potential for complications such as wound dehiscence and infection.